Kostrzewska Anna, Modzelewska Beata, Kleszczewski Tomasz, Batra Satish
Department of Biophysics, Medical University of Bialystok, ul. Mickiewicza 2A, Bialystok, Poland.
Vascul Pharmacol. 2008 Jan;48(1):9-13. doi: 10.1016/j.vph.2007.09.003. Epub 2007 Nov 8.
Nitric oxide (NO) is known to be an important relaxant of contractile activity in various muscles including the human uterine arteries. It has been suggested that NO plays a role in modulation of vascular action of arginin vasopressin (AVP), a strong vasoconstrictor of the human uterine arteries. Therefore, the purposes of this study were to investigate an involvement of endogenous NO in regulation of responses of the human intrauterine arteries to AVP and examine the effect of exogenous NO on contractions of the human intrauterine arteries evoked by AVP. Pretreatment of the artery rings with L-NA, an inhibitor of NO synthase significantly increased the resting force and enhanced the artery responses to AVP. The opposite effect has been observed after administration of 10(-6) mol/L sodium nitroprusside (SNP). Pretreatment of the artery rings with 10(-7) M CTX, a blocker of Ca(2+)-sensitive potassium channels with large conductance, did not change significantly their responses to AVP. Glibenclamide (1.5.10(-6) mol/L), a blocker of ATP-dependent potassium channels and apamin (10(-8) M), a specific blocker of Ca(2+)-sensitive potassium channels with small conductance strongly enhanced the maximum responses of the artery rings to AVP. Pretreatment with CTX significantly decreased the relaxation induced by SNP while apamin attenuated the sensitivity to SNP resulted in rightward shift of the concentration-response curve to SNP. In conclusion, this study indicates that: NO plays a role in regulation of both the vascular tone of the human intramyometrial arteries and their response to AVP. Ca(2+)-sensitive K(+) channels with small and large conductance are involved in the SNP-induced relaxation of these arteries. The pathways of this relaxation cannot be sufficiently explained at this moment and need further investigation.
一氧化氮（NO）是包括人子宫动脉在内的各种肌肉收缩活动的重要松弛剂。有人提出，NO在调节精氨酸加压素（AVP）的血管作用中发挥作用，AVP是人类子宫动脉的强效血管收缩剂。因此，本研究的目的是探讨内源性NO在调节人子宫内动脉对AVP反应中的作用，并研究外源性NO对AVP诱发的人子宫内动脉收缩的影响。用NO合酶抑制剂L-NA预处理动脉环可显著增加静息力，并增强动脉对AVP的反应。给予10（-6）mol/L硝普钠（SNP）后观察到相反的效果。用10（-7）M CTX（一种大电导Ca（2+）敏感钾通道阻滞剂）预处理动脉环，其对AVP的反应无显著变化。格列本脲（1.5.10（-6）mol/L）（一种ATP依赖性钾通道阻滞剂）和蜂毒明肽（10（-8）M）（一种小电导Ca（2+）敏感钾通道特异性阻滞剂）强烈增强动脉环对AVP的最大反应。用CTX预处理可显著降低SNP诱导的舒张，而蜂毒明肽减弱对SNP的敏感性，导致SNP浓度-反应曲线右移。总之，本研究表明：NO在调节人子宫肌层内动脉的血管张力及其对AVP的反应中均起作用。小电导和大电导的Ca（2+）敏感K（+）通道参与了SNP诱导的这些动脉舒张。目前，这种舒张途径尚不能得到充分解释，需要进一步研究。
